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1. Full Text Highly Effective New Treatments for Psoriasis Target the IL-23 Type 17 T Cell Autoimmune Axis
by Kim, Jaehwan and Krueger, James G
Annual Review of Medicine, ISSN 0066-4219, 1/2017, Volume 68, Issue 1, pp. 255 - 269
Psoriasis vulgaris, affecting the skin, is one of the most common organ-specific autoimmune diseases in humans. Until recently, psoriasis was treated by agents... 
IL-17 antagonists | TNF antagonists | psoriasis vulgaris | biologic drugs | IL-23 antagonists | cytokines | polar T cell subsets | pathogenesis of psoriasis | Polar T cell subsets | Psoriasis vulgaris | Cytokines | Pathogenesis of psoriasis | Biologic drugs | MEDICINE, RESEARCH & EXPERIMENTAL | DENDRITIC CELLS | HUMAN SKIN | INNATE LYMPHOID-CELLS | INTERLEUKIN-12/23 MONOCLONAL-ANTIBODY | PHASE-III TRIAL | PLAQUE PSORIASIS | DOUBLE-BLIND | ANTIMICROBIAL PEPTIDE | PLACEBO-CONTROLLED TRIAL | LONG-TERM EFFICACY | Psoriasis - immunology | Interleukin-23 Subunit p19 - antagonists & inhibitors | Psoriasis - drug therapy | Dendritic Cells - immunology | Humans | HLA Antigens - immunology | Dermatologic Agents - therapeutic use | Interleukin-12 Subunit p40 - antagonists & inhibitors | Th17 Cells - drug effects | Interleukin-17 - antagonists & inhibitors | Interleukin-23 - antagonists & inhibitors | Th17 Cells - immunology | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Psoriasis | Interleukins | Physiological aspects | Genetic aspects | Research | T cells | Drug therapy
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2. Full Text Predictors of drug survival for tumour necrosis factor‐α and interleukin 12/23 antagonists in psoriasis
by Egeberg, A
British Journal of Dermatology, ISSN 0007-0963, 08/2016, Volume 175, Issue 2, pp. 247 - 248
Linked Article: Zweegers et al. Br J Dermatol 2016; 175:340–347. 
BIOLOGIC THERAPIES | VULGARIS | DERMATOLOGY | Psoriasis | Humans | Interleukin-12 | Interleukin-23 | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Interleukin-6
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3. Full Text Small-Molecule RORγt Antagonists: One Stone Kills Two Birds
by Zhong, Chao and Zhu, Jinfang
Trends in Immunology, ISSN 1471-4906, 2017, Volume 38, Issue 4, pp. 229 - 231
Although small-molecule thymus-specific isoform of retinoic acid receptor-related orphan nuclear receptor γ (RORγt) antagonists suppressing interleukin... 
Allergy and Immunology | REPERTOIRE | CELLS | MECHANISMS | INHIBITION | DIFFERENTIATION | IMMUNOLOGY | Autoimmunity | Interleukin-17 - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 3 - antagonists & inhibitors | Animals | Interleukin-23 - metabolism | Autoantigens - immunology | Humans | Th17 Cells - immunology | Mice | Thymocytes - immunology | Substance abuse treatment | Cytokines | CD8 antigen | Interleukin | Helper cells | T cell receptors | Lymphocytes T | Inflammation | Gene expression | Thymus | CD4 antigen | Thymocytes | Lymphocytes | Rodents | Ligands | Autoimmune diseases | Retinoic acid | Apoptosis
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4. Full Text Anti cytokine therapy in chronic inflammatory arthritis
by Thompson, Charlotte and Davies, Ruth and Choy, Ernest
Cytokine, ISSN 1043-4666, 10/2016, Volume 86, pp. 92 - 99
This is a review looking at anti cytokine therapy in Rheumatoid Arthritis (RA), Psoriatic Arthritis (PSA) and Ankylosing Spondylitis (AS). The review explores... 
Ankylosing Spondylitis | Rheumatoid Arthritis | Inflammatory arthritis | TNFα inhibitor | Cytokine | IL27 | Psoriatic Arthritis | ACTIVE RHEUMATOID-ARTHRITIS | INADEQUATE RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | PHASE-II | MONOCLONAL-ANTIBODY | ANKYLOSING-SPONDYLITIS | IMMUNOLOGY | PSORIATIC-ARTHRITIS | TOFACITINIB CP-690,550 | PROOF-OF-CONCEPT | CELL BIOLOGY | DOUBLE-BLIND | TNF alpha inhibitor | PLACEBO-CONTROLLED TRIAL | Interleukin-6 - therapeutic use | Cytokines - metabolism | Interleukin-27 - antagonists & inhibitors | Arthritis, Psoriatic - physiopathology | Humans | Spondylitis, Ankylosing - drug therapy | Spondylitis, Ankylosing - physiopathology | Janus Kinases - antagonists & inhibitors | Spondylitis, Ankylosing - immunology | Animals | Arthritis, Psoriatic - immunology | Interleukin 1 Receptor Antagonist Protein - therapeutic use | Interleukin-17 - antagonists & inhibitors | Arthritis, Rheumatoid - drug therapy | Interleukin-23 - antagonists & inhibitors | Arthritis, Psoriatic - drug therapy | Interleukin-12 - antagonists & inhibitors | Mice | Cytokines - antagonists & inhibitors | Arthritis, Rheumatoid - immunology | Arthritis, Rheumatoid - physiopathology | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Chronic Disease - drug therapy | Rheumatoid factor | Arthritis | Psoriasis | Cytokines | Medical colleges | Medical research | Medicine, Experimental
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5. Full Text Suppression of molecular inflammatory pathways by Toll-Like receptor 7, 8, and 9 antagonists in a model of IL-23-induced skin inflammation
by Suaŕez-Fariñas, Mayte and Arbeit, Robert and Jiang, Weiwen and Ortenzio, Francesca S and Sullivan, Tim and Krueger, James G
PLoS ONE, ISSN 1932-6203, 12/2013, Volume 8, Issue 12, p. e84634
Psoriasis is a complex inflammatory disease resulting from the activation of T helper (Th) 1 and Th17 cells. Recent evidence suggests that abnormal activation... 
SIGNALING PATHWAYS | IN-VITRO | MULTIDISCIPLINARY SCIENCES | KERATINOCYTES | EPIDERMAL HYPERPLASIA | ANTIMICROBIAL PEPTIDES | PLASMACYTOID DENDRITIC CELL | EXPRESSION | T-CELLS | PSORIASIS-VULGARIS | INNATE IMMUNITY | RNA, Messenger - immunology | Interleukin-23 - toxicity | Toll-Like Receptor 7 - antagonists & inhibitors | Toll-Like Receptor 9 - antagonists & inhibitors | Dermatitis - immunology | Gene Expression Regulation - immunology | Dermatitis - prevention & control | Gene Expression Regulation - drug effects | Toll-Like Receptor 9 - immunology | Dermatitis - pathology | Signal Transduction - immunology | Toll-Like Receptor 8 - immunology | Animals | Membrane Glycoproteins - antagonists & inhibitors | Toll-Like Receptor 8 - antagonists & inhibitors | Signal Transduction - drug effects | Toll-Like Receptor 7 - immunology | Th17 Cells - immunology | Female | Mice | Membrane Glycoproteins - immunology | Th17 Cells - pathology | Keratin | Psoriasis | Genes | Skin | Inflammation | B cells | Comparative analysis | Gene expression | Dermatitis | Laboratories | Pathogenesis | Hyperplasia | Helper cells | Interleukin 23 | Activation | Antagonists | Lymphocytes T | Kinases | Proteins | Genotype & phenotype | Receptors | Psoriasis vulgaris | Pathways | Lymphocytes | Rodents | Modulation | Toll-like receptors | Skin diseases | Lesions | Growth factors | Immune system | Antigens | Cytokines | Dendritic cells | Dermatology | Injection | Interleukin 17 | Signaling | Aberration | Pharmaceuticals
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6. Full Text Human interleukin‐23 receptor antagonists derived from an albumin‐binding domain scaffold inhibit IL‐23‐dependent ex vivo expansion of IL‐17‐producing T‐cells
by Kuchař, Milan and Vaňková, Lucie and Petroková, Hana and Černý, Jiří and Osička, Radim and Pelák, Ondřej and Šípová, Hana and Schneider, Bohdan and Homola, Jiří and Šebo, Peter and Kalina, Tomáš and Malý, Petr
Proteins: Structure, Function, and Bioinformatics, ISSN 0887-3585, 06/2014, Volume 82, Issue 6, pp. 975 - 989
ABSTRACT Engineered combinatorial libraries derived from small protein scaffolds represent a powerful tool for generating novel binders with high affinity,... 
cytokine | protein scaffold | ribosome display | engineered binding protein | psoriasis | combinatorial library | Protein scaffold | Psoriasis | Engineered binding protein | Combinatorial library | Cytokine | Ribosome display | AUTOIMMUNE INFLAMMATION | HUMAN SERUM-ALBUMIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | COMBINATORIAL LIBRARIES | HIGH-AFFINITY | MONOCLONAL-ANTIBODY | ENGINEERED PROTEINS | STREPTOCOCCAL PROTEIN-G | BIOPHYSICS | INTERFERON-GAMMA | DOUBLE-BLIND | Binding, Competitive | Amino Acid Sequence | Immunologic Factors - chemistry | Receptors, Interleukin - physiology | Anti-Inflammatory Agents - pharmacology | Jurkat Cells | Humans | Bacterial Proteins - chemistry | Molecular Sequence Data | Peptide Fragments - pharmacology | Receptors, Interleukin - antagonists & inhibitors | Sequence Homology, Amino Acid | Peptide Fragments - chemistry | Th17 Cells - drug effects | Anti-Inflammatory Agents - chemistry | Th17 Cells - metabolism | K562 Cells | Interleukin-23 - chemistry | Protein Binding | Drug Evaluation, Preclinical | Interleukin-23 - physiology | Immunologic Factors - pharmacology | Interleukins | Leukemia | Albumin | Chemical properties | T cells | Binding proteins | Protein binding
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7. Full Text Expert opinion on interleukin-12/23 and interleukin-23 antagonists as potential therapeutic options for the treatment of inflammatory bowel disease
by Wong, Uni and Cross, Raymond K
Expert Opinion on Investigational Drugs, ISSN 1354-3784, 05/2019, Volume 28, Issue 5, pp. 473 - 479
Introduction: Blockade of interleukin (IL)-12 and IL-23 is a novel therapeutic target for inflammatory bowel disease (IBD). The monoclonal antibody targeting... 
interleukin-12/23 | ustekinumab | risankizumab | Crohn's disease | ulcerative colitis | brazikumab | guselkumab | inflammatory bowel disease | interleukin-12 | interleukin-23 | mirizumab | Crohn’s disease | MODERATE | SAFETY | MONOCLONAL-ANTIBODY | INDUCTION | SEVERE CROHNS-DISEASE | MAINTENANCE THERAPY | SERUM-LEVELS | DOUBLE-BLIND | PHARMACOLOGY & PHARMACY | ASSOCIATION | Gastrointestinal Agents - pharmacology | Animals | Interleukin-23 - antagonists & inhibitors | Crohn Disease - drug therapy | Humans | Interleukin-12 - antagonists & inhibitors | Ustekinumab - pharmacology | Crohn Disease - physiopathology | Gastrointestinal Agents - adverse effects | Colitis, Ulcerative - drug therapy | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Colitis, Ulcerative - physiopathology
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8. Full Text Upregulation of IL-23 expression in patients with chronic hepatitis B is mediated by the HBx/ERK/NF-κB pathway
by Xia, Limin and Tian, Dean and Huang, Wenjie and Zhu, Hongwu and Wang, Jing and Zhang, Yongguo and Hu, Hao and Nie, Yongzhan and Fan, Daiming and Wu, Kaichun
Journal of Immunology, ISSN 0022-1767, 01/2012, Volume 188, Issue 2, pp. 753 - 764
IL-23 is a newly discovered proinflammatory cytokine that contributes to the maintenance and expansion of Th17 cells. IL-23 has recently been identified as... 
IMMUNE-RESPONSE | ACTIVATION | AUTOIMMUNE INFLAMMATION | INCREASES MIGRATION | IN-VIVO | VIRUS-X PROTEIN | GENE-EXPRESSION | C-REL | INFECTION | IMMUNOLOGY | T-CELLS | Interleukin-12 Subunit p40 - genetics | Interleukin-23 Subunit p19 - antagonists & inhibitors | Hepatitis B, Chronic - immunology | Humans | Middle Aged | Interleukin-23 - blood | Male | Transcriptional Activation - immunology | MAP Kinase Signaling System - immunology | Interleukin-12 Subunit p40 - antagonists & inhibitors | Trans-Activators - physiology | Young Adult | Signal Transduction - immunology | MAP Kinase Signaling System - genetics | Interleukin-23 - antagonists & inhibitors | Interleukin-23 Subunit p19 - genetics | Adult | Female | Inflammation Mediators - antagonists & inhibitors | Hepatitis B, Chronic - pathology | Inflammation Mediators - physiology | Hepatitis B, Chronic - metabolism | NF-kappa B - blood | NF-kappa B - antagonists & inhibitors | Inflammation Mediators - blood | Trans-Activators - blood | Up-Regulation - genetics | Hep G2 Cells | Up-Regulation - immunology | Adolescent | NF-kappa B - physiology | Interleukin-23 - biosynthesis | Promoter Regions, Genetic - immunology | Trans-Activators - antagonists & inhibitors
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9. Full Text Development of the IL‐12/23 antagonist ustekinumab in psoriasis: past, present, and future perspectives – an update
by Yeilding, Newman and Szapary, Philippe and Brodmerkel, Carrie and Benson, Jacqueline and Plotnick, Michael and Zhou, Honghui and Goyal, Kavitha and Schenkel, Brad and Giles‐Komar, Jill and Mascelli, Mary Ann and Guzzo, Cynthia
Annals of the New York Academy of Sciences, ISSN 0077-8923, 08/2012, Volume 1263, Issue 1, pp. 1 - 12
Since the original publication of the article “Development of the IL‐12/23 antagonist ustekinumab in psoriasis: Past, present and future perspectives” in March... 
ustekinumab | psoriasis | safety | Crohn's disease | psoriatic arthritis | human monoclonal antibody | interleukin (IL)‐12/23 | efficacy | Interleukin (IL)-12/23 | Psoriasis | Human monoclonal antibody | Ustekinumab | Efficacy | Safety | Psoriatic arthritis | MULTIDISCIPLINARY SCIENCES | DOUBLE-BLIND | interleukin (IL)-12/23 | PLACEBO-CONTROLLED TRIAL | INTERLEUKIN-12/23 MONOCLONAL-ANTIBODY | Psoriasis - immunology | Psoriasis - drug therapy | Humans | Drug Discovery - trends | Antibodies, Monoclonal - therapeutic use | Drug Discovery - methods | Treatment Outcome | Forecasting | Antibodies, Monoclonal, Humanized | Signal Transduction - immunology | Animals | Interleukin-23 - antagonists & inhibitors | Interleukin-12 - antagonists & inhibitors | Prescription drugs | Crohns disease
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10. Full Text Small intestinal eosinophils regulate Th17 cells by producing IL-1 receptor antagonist
by Sugawara, Reiko and Sugawara, Reiko and Lee, Eun-Jung and Lee, Eun-Jung and Jang, Min Seong and Jang, Min Seong and Jeun, Eun-Ji and Jeun, Eun-Ji and Hong, Chun-Pyo and Hong, Chun-Pyo and Kim, Jung-Hwan and Kim, Jung-Hwan and Park, Areum and Park, Areum and Yun, Chang Ho and Yun, Chang Ho and Hong, Sung-Wook and Hong, Sung-Wook and Kim, You-Me and Kim, You-Me and Seoh, Ju-Young and Seoh, Ju-Young and Jung, YunJae and Jung, YunJae and Surh, Charles D and Surh, Charles D and Miyasaka, Masayuki and Miyasaka, Masayuki and Yang, Bo-Gie and Yang, Bo-Gie and Jang, Myoung Ho and Jang, Myoung Ho
The Journal of experimental medicine, ISSN 0022-1007, 2016, Volume 213, Issue 4, pp. 555 - 567
Eosinophils play proinflammatory roles in helminth infections and allergic diseases. Under steady-state conditions, eosinophils are abundantly found in the... 
IMMUNE | MEDICINE, RESEARCH & EXPERIMENTAL | T(H)17 CELLS | COLONY-STIMULATING FACTOR | EPITHELIAL-CELLS | GM-CSF | INFLAMMATION | INTERLEUKIN-23 | GENERATION | IL-1-BETA | MICROBIOTA | IMMUNOLOGY | Cystinyl Aminopeptidase - genetics | Interleukin-17 - immunology | Interleukin-17 - genetics | Interleukin-1beta - immunology | Mice, Transgenic | Interleukin-1beta - genetics | Eosinophils - immunology | Animals | Intestine, Small - cytology | Cystinyl Aminopeptidase - immunology | Th17 Cells - immunology | Th17 Cells - cytology | Mice | Eosinophils - cytology | Intestine, Small - immunology
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11. Full Text Differential Roles for Interleukin-23 and Interleukin-17 in Intestinal Immunoregulation
by Maxwell, Joseph R and Zhang, Yu and Brown, William A and Smith, Carole L and Byrne, Fergus R and Fiorino, Mike and Stevens, Erin and Bigler, Jeannette and Davis, John A and Rottman, James B and Budelsky, Alison L and Symons, Antony and Towne, Jennifer E
Immunity, ISSN 1074-7613, 10/2015, Volume 43, Issue 4, pp. 739 - 750
Interleukin-23 (IL-23) and IL-17 are cytokines currently being targeted in clinical trials. Although inhibition of both of these cytokines is effective for... 
INFLAMMATORY-BOWEL-DISEASE | CHRONIC PLAQUE PSORIASIS | CROHNS-DISEASE | EPITHELIAL-CELLS | COLITIS | LIPOPOLYSACCHARIDE-BINDING PROTEIN | DOUBLE-BLIND | RECEPTOR COMPLEX | IMMUNOLOGY | T-CELLS | TH17 CELLS | T-Lymphocyte Subsets - immunology | Interleukin-23 Subunit p19 - antagonists & inhibitors | Intestinal Mucosa - physiopathology | ATP Binding Cassette Transporter, Sub-Family B - deficiency | Receptors, Interleukin-17 - immunology | Epithelium - physiopathology | Interleukin-17 - immunology | Interleukin-17 - physiology | Transcriptome | Helicobacter Infections - complications | Interleukin-12 Subunit p40 - antagonists & inhibitors | T-Lymphocytes, Regulatory - immunology | Receptors, Interleukin-17 - physiology | Female | Colitis - drug therapy | Colitis - immunology | Interleukin-23 - physiology | Disease Models, Animal | Gene Expression Regulation - immunology | Immunoglobulin G - therapeutic use | Helicobacter Infections - immunology | Receptors, Interleukin-17 - antagonists & inhibitors | Permeability | Disease Progression | Interleukin-23 - immunology | Mice, Knockout | Colitis - etiology | Animals | Colitis - microbiology | Forkhead Transcription Factors - analysis | Immunization, Passive | Mice | Interleukin-23 Subunit p19 - immunology | Colitis | Psoriasis | Interleukins | Drug resistance | Analysis | Mortality | Inflammatory bowel disease | Studies | Pathology | Flow cytometry | Immunoglobulins | Histopathology | Cytokines | Infections | Inflammation | Gene expression | Crohns disease
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12. Full Text Development of the IL‐12/23 antagonist ustekinumab in psoriasis: past, present, and future perspectives
by Yeilding, Newman and Szapary, Philippe and Brodmerkel, Carrie and Benson, Jacqueline and Plotnick, Michael and Zhou, Honghui and Goyal, Kavitha and Schenkel, Brad and Giles‐Komar, Jill and Mascelli, Mary Ann and Guzzo, Cynthia
Annals of the New York Academy of Sciences, ISSN 0077-8923, 03/2011, Volume 1222, Issue 1, pp. 30 - 39
The development of ustekinumab as a first‐in‐class anti‐interleukin (IL) 12/23p40 therapeutic agent for psoriasis represents an important example of modern and... 
Psoriasis Activity and Severity Index (PASI) | ustekinumab | Dermatology Life Quality Index (DLQI) | human monoclonal antibody (mAb) | Hospital Anxiety and Depression Score (HADS) | psoriasis | Ustekinumab | Psoriasis | Human monoclonal antibody (mAb) | TO-SEVERE PSORIASIS | AUTOIMMUNE INFLAMMATION | CROHNS-DISEASE | IFN-GAMMA | MULTIDISCIPLINARY SCIENCES | INTERLEUKIN-12/23 MONOCLONAL-ANTIBODY | TRIAL | CYTOKINE PROFILE | PLAQUE PSORIASIS | DOUBLE-BLIND | QUALITY-OF-LIFE | Psoriasis - drug therapy | Antibodies, Monoclonal - biosynthesis | Humans | Drug Discovery - trends | Antibodies, Monoclonal - therapeutic use | Forecasting | Interleukin-23 - immunology | Antibodies, Monoclonal, Humanized | Animals | Interleukin-23 - antagonists & inhibitors | Models, Biological | Interleukin-12 - antagonists & inhibitors | Drug Design | Interleukin-12 - immunology | Mice | Immunologic Factors - therapeutic use | Dermatology | Depression, Mental | Immunoglobulin G | Formulae, receipts, prescriptions | Monoclonal antibodies | Dermatologic agents | Anxiety | Rodents
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13. Full Text Induction therapy with the selective interleukin-23 inhibitor risankizumab in patients with moderate-to-severe Crohn's disease: a randomised, double-blind, placebo-controlled phase 2 study
by Feagan, Brian G, Prof and Sandborn, William J, MD and D'Haens, Geert, Prof and Panés, Julián, Prof and Kaser, Arthur, Prof and Ferrante, Marc, Prof and Louis, Edouard, Prof and Franchimont, Denis, Prof and Dewit, Olivier, Prof and Seidler, Ursula, Prof and Kim, Kyung-Jo, Prof and Neurath, Markus F, Prof and Schreiber, Stefan, Prof and Scholl, Paul, MB BChir and Pamulapati, Chandrasena, PhD and Lalovic, Bojan, PhD and Visvanathan, Sudha, PhD and Padula, Steven J, MD and Herichova, Ivona, PhD and Soaita, Adina, PhD and Hall, David B, PhD and Böcher, Wulf O, Prof
Lancet, The, ISSN 0140-6736, 2017, Volume 389, Issue 10080, pp. 1699 - 1709
Summary Background The interleukin-23 pathway is implicated genetically and biologically in the pathogenesis of Crohn's disease. We aimed to assess the... 
Internal Medicine | TRIAL | CELLS | MEDICINE, GENERAL & INTERNAL | ANTI-TNF | INFLAMMATORY-BOWEL-DISEASE | EFFICACY | ULCERATIVE-COLITIS | NECROSIS-FACTOR ANTAGONISTS | ANTITUMOR | MAINTENANCE THERAPY | FACTOR-ALPHA | Severity of Illness Index | Interleukin-23 Subunit p19 - antagonists & inhibitors | Double-Blind Method | Drug Administration Schedule | Humans | Middle Aged | Antibodies, Monoclonal - adverse effects | Gastrointestinal Agents - administration & dosage | Antibodies, Monoclonal - therapeutic use | Male | Treatment Outcome | Remission Induction | Dose-Response Relationship, Drug | Young Adult | Antibodies, Monoclonal - administration & dosage | Crohn Disease - drug therapy | Adolescent | Gastrointestinal Agents - therapeutic use | Adult | Female | Aged | Gastrointestinal Agents - adverse effects | Clinical trials | Monoclonal antibodies | Medicine, Experimental | Medical research | Interleukins | Intravenous administration | Pathogenesis | Mucosa | Interleukin | Interleukin 23 | Antagonists | Intravenous therapy | Randomization | Endoscopes | Motivation | Gastroenterology | Remission | Tumor necrosis factor-TNF | Colon | Safety | Active control | Chronic illnesses | Psoriasis | Cytokines | Ileitis | Nausea | Inflammation | Crohn's disease | Disease control | Patients | Ileum | Crohns disease | Inflammatory bowel disease | Interactive systems | Tumor necrosis factor | Ulcers | TNF inhibitors | Tumors
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